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Int J Mol Sci. 2017 Nov 22;18(11). pii: E2497. doi: 10.3390/ijms18112497.

Quercetin Mitigates Inflammatory Responses Induced by Vascular Endothelial Growth Factor in Mouse Retinal Photoreceptor Cells through Suppression of Nuclear Factor Kappa B.

Lee M1, Yun S2, Lee H3, Yang J4,5,6.

Author information

1
T2B Infrastructure Center for Ocular Disease, Inje University Busan Paik Hospital, Busan 47392, Korea. kamadky@gmail.com.
2
T2B Infrastructure Center for Ocular Disease, Inje University Busan Paik Hospital, Busan 47392, Korea. hyuklips@naver.com.
3
T2B Infrastructure Center for Ocular Disease, Inje University Busan Paik Hospital, Busan 47392, Korea. lhyes0219@gmail.com.
4
T2B Infrastructure Center for Ocular Disease, Inje University Busan Paik Hospital, Busan 47392, Korea. oculoplasty@gmail.com.
5
Department of Ophthalmology, Inje University College of Medicine, Busan 47392, Korea. oculoplasty@gmail.com.
6
EYEBio Korea, Busan 47392, Korea. oculoplasty@gmail.com.

Abstract

Retinal vascular endothelial growth factor (VEGF) increased by neovascularization is well known as a pathogenic factor in ocular neovascular diseases. However, it is still unclear how retinal neurons are damaged by VEGF. The aims of this study are to demonstrate the inflammatory protein expression regulated by VEGF using mouse photoreceptor-derived cells and the protective effect of quercetin against VEGF-induced inflammatory response. Expression and phosphorylation of protein and expression of mRNA were detected by immunoblot and reverse transcriptase polymerase chain reaction. VEGF-induced degradation of limiting membrane and translocation of nuclear factor kappa B (NF-κB) were analyzed by immunocytochemistry. VEGF treatment activated angiogenic signaling pathway in photoreceptor cells. In addition, adhesion molecules and matrix metalloproteinases were increased in VEGF-treated photoreceptor cells. All these events were reversed by quercetin. Zona occludins-1 and β-catenin decreased by VEGF were recovered by quercetin. NF-κB signaling pathway regulated by VEGF through phosphorylations of mitogen-activated protein kinases (MAPK) and protein kinase B (Akt) was suppressed by quercetin. These results suggest that quercetin suppressed VEGF-induced excessive inflammatory response in retinal photoreceptor cells by inactivation of NF-κB signals through inhibition of MAPKs and Akt. These data may provide a basic information for development of pharmaceuticals or nutraceuticals for treatment of retinal diseases caused by excessive VEGF.

KEYWORDS:

VEGF; age-related macular degeneration; diabetic retinopathy; inflammation; photoreceptor; quercetin

PMID:
29165402
PMCID:
PMC5713462
DOI:
10.3390/ijms18112497
[Indexed for MEDLINE]
Free PMC Article

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